- Premature birth/low birth weight
Premature birth (born before 37 weeks of gestation) and low birth weight (less than 2,500 grams) can put the child at a significant risk of developing ADHD. Premature birth usually means that there wasn’t sufficient time for the infant’s brain to develop fully. Leading up to the final weeks of the pregnancy, important parts of the brain, like the prefrontal cortex (the command center of the brain) are undergoing significant development. The immature brains of preterm infants are more vulnerable to injury or irregular development, which can affect the intricate neural networks necessary for attention, impulse control, and hyperactivity regulation. Studies consistently show a higher incidence of ADHD diagnoses in children who were born very prematurely or with very low birth weight. Furthermore, the more prematurely a baby is born (e.g., born at 28 weeks vs. 34 weeks), or the lower their birth weight (e.g., 1000g vs. 2000g), the greater their risk of developing ADHD symptoms later in life.
Various complications during pregnancy and childbirth can also contribute to an increased risk of ADHD. If the mother is exposed to abnormal amounts of stress during the childbirth, or the oxygen supply to the baby’s brain is affected even for a few seconds (Hypoxia), there may be serious implications for the baby’s brain development later in life.
Hypoxia may be caused during childbirth due to complications with the placenta or the umbilical cord. For eg, if the umbilical cord is wrapped around the baby’s head at the time of delivery it may temporarily restrict the oxygen supply. This can potentially damage developing brain cells and neural pathways, thus affecting overall development.
Similarly, prolonged labour or maternal stress may lead to fetal distress thus affecting the nutrient and oxygen supply to the fetus’s brain. This can potentially harm the development of brain structures and neural connections. While pregnancy complications cannot result in ADHD development on their own, they may interact with genetic predispositions and increase the baby’s likelihood of developing ADHD later in life.
- Traumatic Brain Injury (TBI)
Traumatic Brain Injury (TBI), particularly in the formative years of a child’s life can significantly increase the risk or cause ADHD-like symptoms. A TBI involves an external force that injures the brain; this can range from a mild concussion to severe head injury. If the TBI affects the prefrontal cortex or the or pathways involving dopamine and norepinephrine systems, it may cause ADHD-like symptoms.
Even a mild TBI to a young child can result in persistent cognitive and behavioral changes like difficulty maintaining attention, organization, and emotional regulation. As the brain is more vulnerable during early childhood, the age of the child is an important factor in determining the likelihood of ADHD development, along with the severity and location of the injury.
The Role of Epigenetics and Gene–Environment Interaction
Throughout this article, we have mentioned at numerous times that “x” cannot cause ADHD on its own; this is because ADHD is a complex condition that is influenced by multiple factors. These genetic, neurobiological, and environmental factors interact with each other in a unique way. This intricate relationship is often mediated by epigenetics.
Epigenetics refers to the changes in the gene expression that occur without altering the underlying DNA sequence. One may have a particular gene on their DNA sequence, but if this gene is not “read” or activated, it may not be expressed and thus remain inactive. Many chemical components, including the epigenetic ‘marks’ are involved in regulating how the genes are expressed. These epigenetic ‘marks’ are chemical compounds that affect how a gene is “read” from the DNA sequence, thus influencing the gene expression. Epigenetic changes are inheritable, dynamic and potentially reversible; meaning, it is possible to change the gene expression by modifying certain environmental factors.
This gene-environment interaction specifically highlights that the effect of a genetic predisposition can be modified by environmental exposures, and vice versa. For instance, an individual might carry a genetic variant that increases their vulnerability to ADHD, but this vulnerability might only manifest if they are exposed to certain adverse environmental conditions. Conversely, protective environmental factors could potentially mitigate the risk associated with genetic predispositions. Epigenetics underscore the multifactorial nature of ADHD, explaining why genetic or environmental causes alone cannot explain its development.